Evidence map›Paper›PMID 32056100›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2020

Cell Death and Recovery in Traumatic Brain Injury.

Yosuke Akamatsu, Khalid A Hanafy

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 3 pooled it
7.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

102 citing papers in PubMed, 3 syntheses or guidelines pooled it, 179 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. Review
  8. Review
  9. Development of aBioactive materials · 2026
    Article
  10. Article
  11. Review
  12. Article
  13. Article
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  15. Diffuse traumatic brain injury in mice is associated with a transient mismatch of cerebral blood flow and energy metabolism.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Article
  16. Histological investigation of amygdala in horned and hornless ewes.Veterinary research forum : an international quarterly journal · 2026
    Article
  17. CSF1R and IL1R1 inhibitors synergistically attenuate the early pathogenesis of traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  18. Article
  19. Review
  20. Article

42 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Yosuke AkamatsuDivision of Neurosurgery, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Khalid A HanafyDepartment of Neurology, Harvard Medical School, Boston, MA, USA. khanafy@bidmc.harvard.edu.
Harvard University · USIwate Medical University · JP

Funding

Modulation of the TLR4-Lyn interaction in SAHR01NS109174 · NINDS · ROWAN UNIVERSITY · PI HANAFY, KHALID A. · 2019 to 2023
$2.4M
The role of TLR4-dependent sterile inflammation in mediating adverse outcomes after SAHR21NS099606 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HANAFY, KHALID A. · 2017 to 2018
$476k
NINDS NIH HHS R01 NS109174NINDS NIH HHS R21 NS099606
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is the leading cause of morbidity and mortality worldwide. Although TBI leads to mechanical damage during initial impact, secondary damage also occurs as results from delayed neurochemical process and intracellular signaling pathways. Accumulated animal and human studies demonstrated that apoptotic mechanism contributes to overall pathology of TBI. Apoptotic cell death has been identified within contusional brain lesion at acute phase of TBI and in region remote from the site directly injured in days to weeks after trauma. TBI is also dynamic conditions that cause neuronal decline overtime and is likely due to neurodegenerative mechanisms years after trauma. Current studies have even suggested association of neuronal damage through apoptotic pathway with mild TBI, which contributes chronic persistent neurological symptoms and cognitive deficits. Thus, a better understanding of the acute and chronic consequences of apoptosis following TBI is required. The purpose of this review is to describe (1) neuronal apoptotic pathway following TBI, (2) contribution of apoptosis to acute and chronic phase of TBI, and (3) current treatment targeting on apoptotic pathway.

Indexed as

AnimalsApoptosisBrain Injuries, TraumaticHumansNeuronsCell deathRecoveryTraumatic brain injury

Identifiers

PMID32056100
PMCPMC7283441
OpenAlexW3005784714

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.